Pharmacology of psoriasis

Abstract

Although psoriasis is a genetically transferred disease, little is known of the factors causing spontaneous eruption of a proliferative lesion in apparently normal epidermis. Cell kinetic studies indicate an increased epidermal turnover in clinically normal and involved skin, but the pharmacological events regulating epidermopoiesis remain elusive. Possible candidates for the defect in psoriasis are the cyclic nucleotides with their associated enzyme systems. The cyclic AMP: cyclic GMP ratio appears to be reduced in lesional skin. Further phosphodiesterase inhibitors are reported to improve psoriasis. Since prostaglandins stimulate epidermal cyclic AMP in vitro they have been investigated, but with conflicting results. However, the prostaglandins' precursor, arachidonic acid, appears to be elevated in the psoriatic lesion. Epidermal levels of cyclic AMP are also elevated by histamine via H2 receptors and the possibility that histamine exerts a regulatory role needs to be investigated. In conclusion, the pharmacology of psoriasis is complex. Not only do we need to know which pharmacological agents are present in abnormal amounts but more importantly we need to know more about their interactions with one another and with their specific epidermal 'receptors'.